Introduction Intracerebral hemorrhage (ICH) remains a devastating form of stroke. Our understanding of the physiopathology of processes triggered by this disease has improved significantly over the last decade. Nevertheless, effective interventions that are capable of modifying the natural history of the initial and the secondary injury on brain tissue triggered by the hemorrhage are still lacking. Cerebral edema following ICH has received significant attention as a form of secondary neuronal damage. As we begin to better understand the natural history of this form of edema, interventions with potential to ameliorate its burden on these stroke victims are starting to be identified. However, likely due to its close interrelation to the original hematoma volume, its independent effect on neurological function and recovery following ICH is uncertain at best. Pathophysiology Biological events occurring in the periphery of the hematoma following ICH have been the subject of controversy for some years. Initial animal experiments using different models of ICH documented the presence of a rim of ischemia and, in some cases, infarction surrounding the hematoma (1-8). These experiments led to the widely accepted notion of perihematoma cerebral ischemia and they became the rationale for a liberal approach to acute blood pressure control in such stroke patients. Subsequent cerebral blood flow and metabolism studies as well as MRI clinical investigations demonstrated that such perihematoma ischemic condition was far from universal (9-12). Furthermore, these studies demonstrated indirect evidence of perihematoma vasogenic edema, perhaps the result of inflammation, leading to reduced neuronal metabolism. A series of experimental studies have since provided more evidence supporting inflammation as an important component in the process of perihematoma edema development. Microglia and neutrophil infiltration as well as TNF-alpha, IL-1, and free radicals seem to mediate this process (13-18). The expression of these processes also coincides chronologically with the early phases of edema up to its peak. Investigations on the natural history of this form of cerebral edema seem also to suggest that a peak in perihematoma edema volume as large as two to three times the original hematoma volume is reached at approximately 5 days from stroke onset (19-21).
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